AdipoFathttp://adipofat.com
We talk about obesity, nutrition, science,....Tue, 29 Aug 2017 08:32:06 +0000en-UShourly1https://wordpress.org/?v=4.8.2Big datahttp://adipofat.com/big-data
http://adipofat.com/big-data#respondSun, 19 Apr 2015 17:57:47 +0000http://adipofat.com/?p=6112
In 1966 the Statistics Department of North Carolina State University started a research project funded by the National Institute of Health to analyze agricultural data for improving crop yields. They studied variables such as temperature, grain type or fertilizer variety in order to identify patterns that turned out into better harvests. This is one of the stories commonly used to go back to the origins of Big Data, and also the birth of SAS (Statistical Analysis ...]]>CONTRIBUTED BY SILVIA GAMUNDI

In 1966 the Statistics Department of North Carolina State University started a research project funded by the National Institute of Health to analyze agricultural data for improving crop yields. They studied variables such as temperature, grain type or fertilizer variety in order to identify patterns that turned out into better harvests. This is one of the stories commonly used to go back to the origins of Big Data, and also the birth of SAS (Statistical Analysis System), a software for advanced analytics, business intelligence, data management and predictive analytics, that currently holds the largest market-share for advanced analytics.

But, what is Big Data? Why is important? And, who is important for?

Well, the term “big data” was coined in 1997 by Michael Cox and David Ellsworth, two NASA researchers that faced problems with massive amount of information in visualization of Computational Fluid Dynamics, who wrote: “data sets are generally quite large, taxing the capacities of main memory, local disk, and even remote disk. We call this the problem of big data”.

In 2008, the term was popularized with the publication of “Big-Data Computing: Creating revolutionary breakthroughs in commerce, science, and society “, and has acquired a great prominence during last years. However, as McKinsey, and other experts point, there isn’t any rigorous definition for big data, though it could be something close to “the massive analysis of data to take most profit of it and make better future decisions and predictions”.

Either way, when people talks about big data, it is usual to appeal to the three Vs of Big Data defined by industry analyst Doug Laney in 2001: Volume, Velocity and Variety, which are often completed with two more “dimensions”: Veracity and Complexity.

Having or not a clear definition, what it seems clear is the importance it has already reached in many fields so disparate such as banking, insurance, NBA, airlines, social media, or government security, spreading to virtually all areas of life.

Focusing on our field of expertise, big data has is also achieving more and more relevance. In fact, human genome decoding originally took 10 years to process, while now it can be achieved in hours and more than 10,000 times cheaper. We are in the “OMICs” era, and massive analysis, of genes, proteins, metabolites, epigenetics modifications, and hardly everything you could imagine are routinely performed. Tons of information are generated every day, but the real challenge is how to manage it and take most profit out of it, and here is where Big Data strategies come.

Some quick inquests about big data: while writing this post, a pubmed search of the term “big data” retrieved as much as 10 publications so recently added that no abstract was yet available. And maybe more surprising, 112 out of 760 publications with the term “big data” have been published during 2015. Considering that we are just at the beginning of March, and if this tendency keeps on, by the end of the year, the publications related with “big data” DURING 2015 will surpass the total “big data” papers published BEFORE 2015 in pubmed.

And this is just the beginning, according to Gartner Group, in 2015 4.4 million of data scientists will be required worldwide. In fact, Harvard Business Review defined data scientist as “The sexiest job of the 21st century”.

Universities aren’t alien to this phenomenon, in point of fact most renowned universities currently offer MSc programs in big data and data management (LINK).

Experts forecast for big data the same future than the internet had some years ago, it will arrive the day that every single enterprise will have a big data strategy just as it has an Internet one. May be the definition is not so important, but it seems pretty clear that soon will be part of our everyday life. You only need to take a look on Twitter social media, and will see hundreds of new “tweets” released every hour with the tag #bigdata.
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http://adipofat.com/big-data/feed0Benefits of GMOs: Production of human insulinhttp://adipofat.com/benefits-of-gmos-production-of-human-insulin
http://adipofat.com/benefits-of-gmos-production-of-human-insulin#respondSat, 28 Feb 2015 16:15:51 +0000http://adipofat.com/?p=6098
Since its discovery, insulin has become one of the most studied molecules in the history of medicine. As we all know, insulin is a protein related to diabetes, a disease that affects a large percentage of the population. The supply of exogenous insulin is needed to regulate glucose levels in patients with type 1 diabetes in all cases, and occasionally in patients with type 2 diabetes. The Diabetes treatment consists in injecting external insulin to regulate ...]]>Contributed by Elena Torres-Perez

Since its discovery, insulin has become one of the most studied molecules in the history of medicine. As we all know, insulin is a protein related to diabetes, a disease that affects a large percentage of the population. The supply of exogenous insulin is needed to regulate glucose levels in patients with type 1 diabetes in all cases, and occasionally in patients with type 2 diabetes. The Diabetes treatment consists in injecting external insulin to regulate glucose level in blood. Moreover, these patients should maintain a low carbohydrates diet and practice sport.

In 1921, the Canadian physiologists Frederick G. Banting y Charles H. Best extracted the insulin from the dog pancreatic tissue for the first time. Later on, the insulin was obtained from pigs or cows. The problem with this kind of drugs was that they could produce adverse immune reactions in the patients because of the protein was not the same as the human. Others drawbacks of this strategy were the low production yield and the risk of contamination with toxins. For these reasons the pharmaceutical industry decided to produce the human insulin by genetic engineering.

The so-called human insulin is chemically identical to which our body produces, was the first licensed recombinant protein. It was developed by Genentech and marketed by Ely Lilly in 1982.

At present, insulin is being produced mainly in Escherichia coli y Saccharomyces cerevisiae for the treatment of diabetic patients. The bacteria, specifically E. coli, are used to synthesize the A and B human insulin chains separately. The genes which encode these proteins are introduced by pBR322 vector. Afterwards, it is carried out the purification, in vitro folding and union of the both chains. The union is performed by the oxidation of cysteins to shape the disulphide bounds of the active protein. E. coli offers several advantages such as high growth rate, simple media requirement, easy to handle, high yield and cost-effectiveness. Nevertheless, there are disadvantages such as loss of plasmid and antibiotic property, unsolicited inducers for genes expression, intracellular accumulation of heterologous proteins as inclusion bodies, improper protein refolding and lack of post-translational modifications, endotoxin contamination, poor secretion and proteolytic digestion. In E. coli, the protein can be secreted in the periplasm, which has advantages over cytoplasm, improving the protein production and purification.

On the other hand, the yeast cells yield soluble insulin precursors which are secreted into the culture supernatant. The synthesis of insulin in yeast cells allows the insertion of numerous post-translational modifications. However, the main problem for producing therapeutic glycoprotein for human application is that the yeast N-glycosilation is of the high mannose type, which makes the protein less effective due to a short half-life and the hyper-immunogenicity produced. Besides S. cerevisiae, alternative yeast strains have been investigated and it has been found that Pichia pastoris could be an attractive option for large-scale production of recombinant insulin.

Furthermore E. coli and yeast, mammalian cells, transgenic animal and plant expression system are also employed as a host for large-scale production of recombinant production. The use of transgenic plants has many advantages such as cost effectiveness, high quality protein processing and absence of human pathogens, ease production and presence of eukaryotic machinery for posttranslational modifications. Specifically, recombinant human insulin has been expressed in oilseeds of plant Arabidopsis thaliana getting very high level of expression with easy recovery.

In conclusion, there are different ways of producing recombinant human insulin and nowadays the aim is to improve the expression of insulin using different host cell.
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http://adipofat.com/benefits-of-gmos-production-of-human-insulin/feed0The good fathttp://adipofat.com/the-good-fat
http://adipofat.com/the-good-fat#respondSun, 15 Feb 2015 11:35:56 +0000http://adipofat.com/?p=6086
Obesity is defined as an excess of body fat tissue. Adipose tissue (white adipose tissue) is the organ whose main function is to store the overflow of energy from the diet. The body mass index (BMI) is a quick formula to know when an individual person is obese, being 25 kg/m2 and 30 kg/m2 the overweight and obesity thresholds, respectively..
Anatomically, the white adipose tissue is present in three big discrete body depots. The big one ...]]>Contributed by Sergio Perez-Diaz

Obesity is defined as an excess of body fat tissue. Adipose tissue (white adipose tissue) is the organ whose main function is to store the overflow of energy from the diet. The body mass index (BMI) is a quick formula to know when an individual person is obese, being 25 kg/m2 and 30 kg/m2 the overweight and obesity thresholds, respectively..

Anatomically, the white adipose tissue is present in three big discrete body depots. The big one is the subcutaneous fat tissue (SAT), which stores up to 80% of total body lipids. The most commonly studied, the subcutaneous depot is central-abdominal. Intra-visceral (VAT) fat depot is an inner central-abdominal region that represents 10-20% of total body fat in men and a 5-10% in women. Moreover, there are smaller specialized adipose tissue depots such as, pericardial or intramuscular. Recently was discovered the presence of brown adipose tissue in human adults. Its localization was centered in cervical, perirenal and paravertebral regions with myogenic or trans-differentiation from white adipose tissue origins. Its function is burn fats so knowledge is in focus of researchers to fight against obesity.

High heterogeneity in morphology, cell composition, metabolism or hormonal function exists in each regional depot. Generally, adipocytes are smaller in visceral fat tissue. The non-adipocyte cell number is higher in VAT (with a population of innate system cells, according with the elevated secretion of pro-inflammatory cytokines) than SAT, which contains higher number of precursors of adipocytes and secretion of pro-adiposity adipokines as leptin or adiponectin. The release (lipolysis) and uptake (lipogenesis) of triglycerides of fatty acids to control lipids and carbohydrate homeostasis, is controlled by fat tissue. Adipocytes from SAT have more adipogenesis/lipogenesis markers and lipids stored than VAT adipocytes. The rate of lipolysis is higher in central fat (VAT > SAT) and low in SAT lower body fat.

Genetics, as well as environmental factors has played a role in regional differences of fat storage and distribution in different human populations. It is not difficult to understand the environmental differences between bushmens and inuits in terms of percentage of fat tissue as isolation layer. The size of stores is variable from 5 to 60% of total body weight. There is a worldwide variation of obesity ranging; from India, where 3-4% of the population is obese, until the 80% in some Pacific Island regions. In addition to environmental factors, its susprising how a single mutation in a single gene , as leptin or leptin receptor , lead in rare obesity or how two hours of additional TV Increased 2% of the obesity prevalence.

The evolutionary function of the fat tissue is release nutrients in hunger seasons and stores the nutrients at seasons with excess of food. Today, the genetic obesity factor of each race or region marked by the environment has been blocked by the economic and cultural side of the human society. Excessive caloric intake and so-called junk food in Western countries and absence hunger season in less developed countries made that, the prevalence of obesity in almost all countries was increased in the last years. The world Health organization has estimated that for this year 2015, 2.3 billion and 700 million of people will be overweight or obese respectively.

All obese individuals have in common an elevated percentage of fat tissue. However, fat distribution is highly variable among obese individuals. Recent studies around the world, shown as obese Asians have more central adiposity (VAT and SAT) than Caucasians, and African Americas and Hispanics have relatively less central VAT, but more fat mass than them in percentage. Women have a tendency higher to adiposity than men. In addition, men accumulate more fat in abdominal area and women in lower body. This distribution was canonical named like apple and pear.

About 20-30% of adult population has problems associated with overweight, as Metabolic syndrome (Mets). Classically, Mets is a group of clustered events in individual patients such as: obesity, inflammation, insulin resistance, blood lipids disorders and increased risk of developing cardiovascular disease. Not all obese have the same distribution and size of fat mass and not all obese individuals develop metabolic syndrome. It is known, that different depots lead different quality of life. The general pattern to identifying a patient of Mets, is today unknown but central-abdominal VAT, is the clearest manifestation of Mets.

Now, we know that the SAT (perigluteal in women and elevated ratio, subcutaneous/visceral depots in abdominal fat in men) have “healthy” functions buffering the effect of co-morbidities. Meanwhile, an elevated level of VAT depots raises the risk of suffering metabolic syndrome. For example, the prevalence of diabetes is greater in men than women, likely because femoral SAT storage in women has a healthier role than abdominal fat in men.An interesting view to understand how different depots of Fat tissue changes the prevalence to suffer MetS could be documented in U.S.A. The capacity to gain weight and becoming in obese is lower in American Asians, American Whites and American Blacks is in this order. However, the prevalence of problems associated with the obesity, taken the same BMI in this groups is bigger in American Asians than Blacks. This may be explained because was measure that obese Asians have a low ratio of SAT/VAT than American Blacks. Moreover, MetS is associated with aging. This is due to slower metabolism, together abdominal lipid storage in both sex.

Many theories exist to correlate visceral fat with MetS. The body’s ability to cope with the surplus of calories could determine the susceptibility to developing MetS. If this surplus of energy-dense food or/and lack of physical activity is stored by an insulin-responsive adipose tissue SAT, the gain of weight will be healthy. But, if this surplus is shipped into a dysfunctional SAT unable to expand, this excess of energy will diverted for storage in the visceral fat tissue. The features of VAT, leads abdominal dysfunctional storage of fats and in the end, an ectopic fat depot (as muscle, heart or liver) and presence of clinical Mets.

This knowledge opens a new focus to try to cure, treat or prevent Mets, looking for molecular markers that determine dysfunctional fat tissue and targets to promote the good fat.

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http://adipofat.com/the-good-fat/feed0US Burden of diseasehttp://adipofat.com/us-burden-of-disease
http://adipofat.com/us-burden-of-disease#respondTue, 13 Aug 2013 06:23:39 +0000http://adipofat.com/?p=5981
The United States spends the most per capita on health care across all countries, yet lacks universal health coverage, and lags behind other high-income countries for life expectancy. and many other health outcome measures.From 1990 to 2010, the US made substantial progress in improving health. Life expectancy increased and all-cause death rates at all ages decreased. However, morbidity and chronic disability now account for nearly half of the US health burden, and improvements in population health in the US are slower than ...]]>
The United States spends the most per capita on health care across all countries, yet lacks universal health coverage, and lags behind other high-income countries for life expectancy. and many other health outcome measures.From 1990 to 2010, the US made substantial progress in improving health. Life expectancy increased and all-cause death rates at all ages decreased. However, morbidity and chronic disability now account for nearly half of the US health burden, and improvements in population health in the US are slower than for many other high-income countries.

In this report, burden of disease in the US has been studied to determine how these health burdens have changed over the last 2 decades, and to compare the United States with other Organisation for Economic Co-operation and Development (OECD) countries. This infographic from the Best Master of Science in Nursing Degrees summarizes it very nicely

]]>http://adipofat.com/us-burden-of-disease/feed0Cochrane meta-anaylisis about Diet & Cardiovascular Diseasehttp://adipofat.com/cochrane-meta-anaylisis-about-diet-cardiovascular-disease
http://adipofat.com/cochrane-meta-anaylisis-about-diet-cardiovascular-disease#commentsThu, 10 Jan 2013 22:04:55 +0000http://adipofat.com/?p=5829
The Cochrane Collaboration is an international network that, using the meta-analysis method, analyzes randomized clinical trials (RCT) available on various subjects, and synthesizes them into regularly updated systematic reviews. The information ...]]>meta-analysis is a statistical method in which results of individual studies are mathematically combined in order to improve the reliability of the results. This technique presents enormous advantages over classical literature reviews. Meta-analyses also present weaknesses and they are fundamentally limited by the quality of the underlying studies.
The Cochrane Collaboration is an international network that, using the meta-analysis method, analyzes randomized clinical trials (RCT) available on various subjects, and synthesizes them into regularly updated systematic reviews. The information found in Cochrane is considered by many to be the Gold Standard to evaluate drug therapy for treating disease.Additionally, meta-analysis of several small studies does not predict the results of a single large study, especially in a field like medicine where results are truly unpredictable [1].
It is debatable whether or not the Cochrane methodology is adequate for the nutrition questions in medical practice. It has been argued that more of the evidence base in nutrition is observational and a strict rule for excluding all non-RCT evidence would prevent many relevant studies from being included in the analysis [2]. Likewise, some argue that randomization would not be important for dietary experiments in which all participants are exposed to the same experimental diet [3]. Cochrane authors rebutted these criticisms by stating that cohort or non-randomized trials suffer the problems of bias and confounding [4]. Confounding arises because of clustering of dietary behaviors with other ‘healthy’ lifestyle attributes – those who eat less saturated fat or salt are more likely to be wealthier, better educated, have better social support, be non-smokers, take sufficient physical activity and eat plenty of fruit, vegetables, nuts, whole grains, low-fat dairy food, etc. Adjusting for a handful of these components does not guarantee complete control of such confounding.
All the above can be summarized by saying that Cochrane meta-analysis are, undoubtedly, the most prestigious systematic reviews on the medical field. Here we sumarize some information compiled by Cochrane guys to debunk some diet myths and learn the truth about eating healthfully. However, caution must be exercised (as always) when drawing inferences from the results of these studies.

DIET & CARDIOVASCULAR DISEASE

Reduced dietary salt for the prevention of cardiovascular disease (January,2011)

This review was aimed to 1)assess the long term effects of reducing dietary salt on mortality and cardiovascular morbidity and 2) investigate whether blood pressure reduction is an explanatory factor on mortality and cardiovascular outcomes.
Seven studies (including 6,489 participants) met the inclusion criteria – three in normotensives (n=3518), two in hypertensives (n=758), one in a mixed population of normo- and hypertensives (n=1981) and one in heart failure (n=232) with end of trial follow-up of seven to 36 months and longest observational follow up (after trial end) to 12.7 yrs. Relative risks for all cause mortality in normotensives and hypertensives showed no strong evidence of any effect of salt reduction. Cardiovascular morbidity in people with normal blood pressure or raised blood pressure at baseline also showed no strong evidence of benefit. Salt restriction increased the risk of all-cause death in those with congestive heart failure. The authors concluded that there is still insufficient power to exclude clinically important effects of reduced dietary salt on mortality or cardiovascular morbidity in normotensive or hypertensive populations. Further evidence is needed to confirm whether restriction of sodium is harmful for people with heart failure.(+)

Dietary advice for reducing cardiovascular risk (January, 2009)

Thirty-eight trials comparing dietary advice with no advice were included in the review. Dietary advice reduced total serum cholesterol and LDL cholesterol after 3-24 months. Mean HDL cholesterol levels and triglyceride levels were unchanged. Dietary advice reduced blood pressure and 24-hour urinary sodium excretion. Three trials reported small increases in plasma antioxidants. Compared to no advice, dietary advice increased fruit and vegetable intake by 1.25 servings/day. Dietary fiber intake increased with advice while total dietary fat ,as a percentage of total energy intake, fell by 4.49 % and saturated fat intake fell by 2.36 %.
Dietary advice did appear to be effective in bringing about modest beneficial changes in diet and cardiovascular risk factors over approximately 10 months but the trials did not manage to answer the question of whether the beneficial changes in cardiovascular risk factors resulted in a reduced incidence of heart disease, stroke, or heart attack. (+)

This updated review suggested that modifying dietary fat (not reducing fat from the diet) decreased the risk of cardiovascular events in trials of, at least, two years duration and in studies of men (not of women). However, there were no significant effects of dietary fat changes on total mortality (RR 0.98, 95% CI 0.93 to 1.04, 71,790 participants) or cardiovascular mortality (RR 0.94, 95% CI 0.85 to 1.04, 65,978 participants). (+)

Forty eight randomised controlled trials (36,913 participants) and 41 cohort analyses were included. Pooled trial results did not show a reduction in the risk of total mortality or combined cardiovascular events in those taking additional omega 3 fats
Restricting analysis to trials increasing fish-based omega 3 fats, or those increasing short chain omega 3s, did not suggest significant effects on mortality or cardiovascular events in either group. Subgroup analysis by dietary advice or supplementation, baseline risk of CVD or omega 3 dose suggested no clear effects of these factors on primary outcomes. (+)

This review is an update of all relevant randomised trials that have evaluated an intervention that aimed to reduce more than one risk factor (high cholesterol, excessive salt intake, high blood pressure, excess weight, a high-fat diet, smoking, diabetes and a sedentary lifestyle) in people without evidence of cardiovascular disease. The findings are from 55 trials of between six months and 12 years duration conducted in several countries over the course of four decades. Multiple risk factor intervention does result in small reductions in risk factors including blood pressure, cholesterol and smoking. Contrary to expectations, multiple risk factor interventions had little or no impact on the risk of coronary heart disease mortality or morbidity. This could be because these small risk factor changes were not maintained in the long term. Alternatively, the small reductions in risk factors may be caused by biases in some of the studies. The methods of attempting behavior change in the general population are limited and do not appear to be effective.(+)

]]>http://adipofat.com/cochrane-meta-anaylisis-about-diet-cardiovascular-disease/feed1Estimation of Risk for Child or Adolescent Obesity at Birthhttp://adipofat.com/estimation-of-risk-for-child-or-adolescent-obesity-at-birth
http://adipofat.com/estimation-of-risk-for-child-or-adolescent-obesity-at-birth#respondWed, 02 Jan 2013 17:27:37 +0000http://adipofat.com/?p=5819
When the performance of genetics in predicting early obesity phenotypes was explored, with the largest list of obesity-SNPs ever used, it showed only ...]]>GWAS’s coffin.
And the formula?…well, it does not seem very complicated to me.
It only looks at only six factors: Parental BMI, birth weight, maternal gestational weight gain, number of household members, maternal professional category and smoking habits .
Morandi A, Meyre D, Lobbens S, Kleinman K, Kaakinen M, et al. (2012) Estimation of Newborn Risk for Child or Adolescent Obesity: Lessons from Longitudinal Birth Cohorts. PLoS ONE 7(11): e49919. doi:10.1371/journal.pone.0049919
]]>http://adipofat.com/estimation-of-risk-for-child-or-adolescent-obesity-at-birth/feed0Is the Obesity Paradox an actual paradox ?http://adipofat.com/is-the-obesity-paradox-an-actual-paradox
http://adipofat.com/is-the-obesity-paradox-an-actual-paradox#respondFri, 28 Dec 2012 17:51:28 +0000http://adipofat.com/?p=58061). Yet, the term “obesity paradox” was coined by Gruberg (2) who found that patients with known coronary artery disease and BMI within the normal range (<25 kg/m2) who undergo percutaneous coronary intervention are at the highest risk for in-hospital complications and for increased one-year mortality. The evidence that being overweight or obese is associated with lower mortality has been demonstrated in individuals with heart failure (3) , established coronary artery disease (4) and in a range of cardiovascular disease (CDV) conditions up till today (5), as well as in several non CDV conditions [Reviewed in (6)]. This paradox is explained by some people stating that a BMI of ∼25–35 kg/m2 benefits patients with chronic disease because excess fat serves as an energy depot in times of need.
If you are overweight, the most effective thing you can do to prevent diabetes is to lose weight. Right? . However, in the last twist of this not-quite-paradoxical obesity paradox, three very recent studies might disagree. Based on data from 2625 US individuals with incident diabetes (7), when compared with overweight and obese individuals, those who are normal weight at the time of diabetes incidence have higher mortality rates. Additionally, 89,056 Taiwanese individuals with type 2 diabetes where followed for 12 years (8). In all, 30.3% died during follow-up period. Increased risk of death was associated with older age, longer duration with diabetes, using insulin, male sex, hypertension, smoking and lower BMI. Age, sex and risk adjusted hazard ratios demonstrated reduced risk of all-cause mortality with increasing category of BMI, all the way from underweight, to class II obesity. Likewise, weight loss does not reduce cardiovascular events in people with longstanding type 2 diabetes, according to The Look AHEAD study supported by the National Institutes of Health ( more information in www.lookaheadtrial.org ).
All these studies lead to my reflection. My take-home message. There really is no such a thing as obesity. There are many “obesities”. Obesity may (or may not) predispose to developing a number of health problems. Once those problems have developed, some obese patients may have a survival advantage over patients who are not. Obesity comes thence in many different flavors. We, as scientists, must find a way to differentiate those obesities.
1. P. Degoulet et al., Mortality risk factors in patients treated by chronic hemodialysis, Nephron31, 103–110 (1982).
2. L. Gruberg et al., The impact of obesity on the short-term and long-term outcomes after percutaneous coronary intervention: the obesity paradox?, Journal of the American College of Cardiology39, 578–84 (2002).
3. A. Oreopoulos et al., Body mass index and mortality in heart failure: a meta-analysis., American heart journal156, 13 (2008).
4. A. Romero-Corral et al., Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies, The Lancet368, 666–678 (2006).
5. O. Angerås et al., Evidence for obesity paradox in patients with acute coronary syndromes: a report from the Swedish Coronary Angiography and Angioplasty Registry, European Heart Journal (2012) .
6. P. A. McAuley, S. N. Blair, Obesity paradoxes, Journal of Sports Sciences29, 773–782 (2011).
7. M. R. Carnethon et al., Association of Weight Status With Mortality in Adults With Incident Diabetes, JAMA308, 581–590 (2012).
8. C. H. Tseng, Obesity paradox: differential effects on cancer and noncancer mortality in patients with type 2 diabetes mellitus, Atherosclerosis (2012).
]]>http://adipofat.com/is-the-obesity-paradox-an-actual-paradox/feed0JAMA>Opportunities to Reduce Childhood Hunger and Obesity Restructuring the Food Stamp Programhttp://adipofat.com/jamaopportunities-to-reduce-childhood-hunger-and-obesity-restructuring-the-food-stamp-program
http://adipofat.com/jamaopportunities-to-reduce-childhood-hunger-and-obesity-restructuring-the-food-stamp-program#respondWed, 26 Dec 2012 22:29:31 +0000http://adipofat.com/jamaopportunities-to-reduce-childhood-hunger-and-obesity-restructuring-the-food-stamp-program
David S. Ludwig, MD, PhD; Susan J. Blumenthal, MD, MPA; Walter C. Willett, MD, DrPH
JAMA. 2012;308(24):2567-2568. doi:10.1001/jama.2012.45420.
Childhood is a time of substantial nutritional needs. However, many children in low-income families do not consume adequate amounts of nutritious foods for optimal physical development, cognitive performance, and psychological well-being. The pending reauthorization of the Supplemental Nutrition Assistance Program (SNAP, formerly known as the ...]]>
Strayer M, Eslami E, Leftin J. Characteristics of Supplemental Nutrition Assistance Program Households: Fiscal Year 2011. Alexandria, VA: US Dept of Agriculture, Food and Nutrition Service, Office of Research Analysis; 2012
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Kursmark M, Weitzman M. Recent findings concerning childhood food insecurity. Curr Opin Clin Nutr Metab Care. 2009;12(3):310-316
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Coleman-Jensen A, Nord M, Andrews M, Carlson S. Household Food Security in the United States in 2011. Washington, DC: US Dept of Agriculture; September 2012. Economic Research Service report ERR-141. http://www.ers.usda.gov/media/884525/err141.pdf. Accessed December 3, 2012
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Nord M, Andrews M, Carlson S. Food Security in the United States, 2008. Washington, DC: Economic Research Service, US Dept of Agriculture; November 2009. USDA publication ERR-83. http://www.ers.usda.gov/media/257321/err83fm_1_.pdf. Accessed November 28, 2012
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Zhang LN, Mitchell SE, Hambly C, Morgan DG, Clapham JC, Speakman JR. Physiological and behavioral responses to intermittent starvation in C57BL/6J mice. Physiol Behav. 2012;105(2):376-387
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Shenkin JD, Jacobson MF. Using the Food Stamp Program and other methods to promote healthy diets for low-income consumers. Am J Public Health. 2010;100(9):1562-1564
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Polhemus B, Dalenius K, Mackintosh H, Smith B, Grimmer-Strawn L. Pediatric Nutrition Surveillance 2009 Report. Atlanta, GA: US Dept of Health and Human Services, Centers for Disease Control and Prevention; 2011
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Blumenthal SJ, Hoffnagle E, Willet W, et al. SNAP to Health: A Fresh Approach to Strengthening the Supplemental Nutrition Assistance Program. 2012. Washington, DC: Center for the Study of the Presidency and Congress; July 2012. http://www.thepresidency.org/storage/documents/CSPC_SNAP_Report.pdf. Access November 28, 2012
]]>http://adipofat.com/jamaopportunities-to-reduce-childhood-hunger-and-obesity-restructuring-the-food-stamp-program/feed0SATURATED FAT AND CARDIOVASCULAR DISEASEhttp://adipofat.com/saturated-fat-and-cardiovascular-disease
http://adipofat.com/saturated-fat-and-cardiovascular-disease#respondThu, 13 Dec 2012 17:54:12 +0000http://adipofat.com/?p=5374
–The saturated fat content of the diet is NOT associated with cardiovascular disease. A systematic review of 146 prospective ...]]>
–The saturated fat content of the diet is NOT associated with cardiovascular disease. A systematic review of 146 prospective cohort studies describing 361 subcohorts and 43 randomized clinical trials (RCT) involving 51 subgroups did not find evidence supporting a causal link between dietary saturated fatty acids or total fat and Coronary Heart Disease (CHD)[1]. Likewise a meta-analysis of 21 studies prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD [2].
–The reduction of the percentage of fat in the diet does NOT reduce the incidence of cardiovascular disease. One meta-analysis, pooling 8 clinical trials described that replacement of some dietary saturated fat with PUFA reduces CHD and that the benefits associated with PUFA consumption increased with longer duration of the trials[3]. The Cochrane Collaboration is an international network of individuals and institutions that review and analyze the best clinical trials available on various subjects, and synthesize them into regularly updated systematic reviews. The information found in Cochrane is considered by many to be the Gold Standard. When the prevention of CVD through reduction or modification of dietary fat was addressed with a meta-analysis of 48 RCT, their review suggested that modification (not reduction), of at least two years duration and in studies of men (not of women), decreased the risk of cardiovascular events. More importantly, there were no clear effects of dietary fat changes on total mortality[4].
Where we stand now: Industrially produced trans fatty acids (TFAs) are consistently associated with a higher risk of CVD (on a gram-for-gram basis) and meta-analyses of cohort studies state that saturated fat intakes are not associated with CHD, stroke, or CVD.

]]>http://adipofat.com/saturated-fat-and-cardiovascular-disease/feed01st posthttp://adipofat.com/1st-post
http://adipofat.com/1st-post#commentsMon, 09 Jan 2012 18:03:30 +0000http://adipofat.com/?p=5289
However, this is what you get.
Do not fret, good posts will follow.
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Do not fret, good posts will follow.
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